| Project/Area Number |
16K19156
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Immunology
|
|---|
| Research Institution | Kobe University |
|---|
Principal Investigator |
KASAGI SHIMPEI 神戸大学, 医学部附属病院, 特定助教 (80457051)
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
|---|
| Keywords | 制御性T細胞 / 動脈硬化 / 抗原特異的免疫抑制療法 / 制御性Ｔ細胞 / HSP65 / 抗原特異性 / 免疫抑制療法 / 循環器・高血圧 / 免疫学 |
|---|
| Outline of Final Research Achievements |
In the HSP65 (endothelial antigen) derived arterosclerosis model mice, we found that combination therapies of HSP65 antigen and B cell depletion suppressed antigen specific lymphocyte proliferation and cytokine production such as MCP-1, IL-6, TNF-alpha, IL-10. Eventually, development of arterosclerosis was strongly suppressed by these combination therapies.HSP65 specific regulatory T cells and regulatory B cells were induced after combination therapies, which was triggered by TGF-beta produced by macrophages. B cell depletion alone or HSP65 antigen alone did not suppress arteriosclerosis.
|
